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The Role of Vagal Nerve Root Injury on Respiration Disturbances In Original Investigation Original Received: 03.12.2013 / Accepted: 11.02.2014 DOI: 10.5137/1019-5149.JTN.9964-13.1 The Role of Vagal Nerve Root Injury on Respiration Disturbances in Subarachnoid Hemorrhage Subaraknoid Kanamada Solunum Bozuklukları Oluşmasında Vagal Sinir Kökü Hasarının Rolü Murteza CAKıR1, Canan AtALAY 2, Zeynep CAKıR3, Mucahit Emet3, Mehmet Dumlu AYDıN1, Nazan AYDıN4, Arif ONDER5, Muhammed CAlıK6 1Ataturk University, School of Medicine, Department of Neurosurgery, Erzurum, Turkey 2Ataturk University, School of Medicine, Department of Anesthesiology and Reanimation, Erzurum, Turkey 3Ataturk University, School of Medicine, Department of Emergency Medicine, Erzurum, Turkey 4Ataturk University, School of Medicine, Department of Psychiatry, Erzurum, Turkey 5Avrasya Hospital, Department of Neurosurgery, Istanbul, Turkey 6Ataturk University, School of Medicine, Department of Pathology, Erzurum, Turkey Corresponding Author: Murteza CAKır / E-mail: [email protected] ABSTRACT AIM: We examined whether there is a relationship between vagal nerve root injury and the severity of respiration disorders associated with subarachnoid hemorrhage (SAH). MaTERIAL and METHODS: This study was conducted on 20 rabbits. Experimental SAH was induced by injecting homologous blood into the cisterna magna. During the experiment, electrocardiography and respiratory rhythms were measured daily. After the experiment, any axonal injury or changes to the arterial nervorums of the vagal nerves were examined. All respiratory irregularities and vagal nerve degenerations were statistically analyzed. RESULTS: Normal respiration rate, as measured in the control group, was 30±6 bpm. In the SAH-induced group, respiration rates were initially 20±4 bpm, increasing to 40±9/min approximately ten hours later, with severe tachypneic and apneic variation. In histopathological examinations, axon density of vagal nerves was 28500±5500 in both control and sham animals, whereas axon density was 22250±3500 in survivors and 16450±2750 in dead SAH animals. The severity of axonal degeneration of vagal nerves was greater in the six dead animals than in the survivors. CONCLUSION: If vagal nerves are lesioned, the muscles of respiration are paralyzed and respiratory reflexes are disrupted. That the ischemic and mechanical factors created by SAH cause vagal nerve root injury and respiration disorders may be inevitable and fatal. KEYWORDS: Injury, Respiration, Rabbit, Subarachnoid hemorrhage, Vagal nerve ÖZ AMAÇ: Subaraknoid kanamada (SAK) solunum bozukluklarının şiddetiyle vagal sinir kökü hasarı arasında bir ilişki olup olmadığını inceledik. YÖNTEM ve GEREÇLER: Çalışma 20 tavşanda gerçekleştirildi. Sisterna magnaya homolog kan enjeksiyonuyla deneysel SAK oluşturuldu. Deney sırasında günlük olarak elektrokardiyografi ve solunum ritimleri ölçümü yapıldı. Deneyden sonra, vagal sinirlerin arteriyel nervorumlarındaki değişiklikler ve varsa aksonal hasar incelendi. Tüm solunum düzensizlikleri ve vagal sinir dejenerasyonları istatistiksel olarak analiz edildi. BULGULAR: Kontrol grubunda ölçüldüğü şekilde normal solunum hızı 30±6 dk şeklindeydi. SAK indüklenmiş grupta solunum hızları başlangıçta 20±4 dk iken, on saat sonrasında şiddetli takipneik ve apneik varyasyonla 40±9/dk değerine yükseldi. Histopatolojik incelemelerde vagal sinirlerin akson yoğunluğu hem kontrol hem taklit (sham) deneklerinde 28500±5500 iken yaşayan SAK deneklerinde 22250±3500 ve ölü SAK deneklerinde 16450±2750 bulundu. Vagal sinirlerde aksonal dejenerasyonun şiddeti 6 ölü denekte yaşayanlardan daha fazlaydı. SONUÇ: Vagal sinirlerde lezyon oluşursa, solunum kasları felce uğrar ve solunum refleksleri bozulur. SAK’nın oluşturduğu iskemik ve mekanik faktörlerin vagal sinir kök hasarı ve solunum bozuklukları oluşturması kaçınılmaz ve ölümcül olabilir. ANAHTAR SÖZCÜKLER: Hasar, Solunum, Tavşan, Subaraknoid kanama, Vagal sinir INTRODUCTION from the lower brainstem, cervical and thoracic segments Respiration can be defined as a process of gas exchange in the and surround the respiration muscles, pleural and thoracic lungs via inspiratory and expiratory drives (7, 21). Respiratory surfaces, and play a major role in the conscious continuation organs are innervated by somatic and autonomic nervous of respiration (21). Autonomic nerves control the caliber of systems (24). The somatic sensitive-motor nerves arise the conducting airways, pulmonary blood vessels, the volume Turk Neurosurg 2015, Vol: 25, No: 2, 273-278 273 Cakir M. et al: Vagal Nerve Root Injury in Subarachnoid Hemorrhage of respiratory units, the activity of bronchial glands and Xylazine HCL, 30 mg/1.5 mL; and distilled water, 1 mL) was respiration reflexes. The vagal nerve is the principle neural subcutaneously injected immediately before surgery. All pathway that interconnects the brainstem and the lungs. It animals were monitored for electrocardiographic changes, is involved in maintaining the rhythm of central respiration, respiration patterns, and blood oxygen concentrations and regulation of the pulmonary vasculature, airways and during the procedures. All parameters were recorded by Sony pulmonary secretion (8). Activation of the pulmonary stretch camera and were analyzed by physicians who were blinded receptors by lung inflation or vagal stimulation evokes the to study. During the operation, 0.1 mL/kg of anesthetic Hering-Breuer reflex, which is characterized by inspiratory combination was used as required. For the SAH group, 0.75 mL inhibition and expiratory prolongation (13). Stimulation of of autologous blood was taken from the auricular artery and the vagal nerve can cause bronchoconstriction, respiration injected into the cisterna magna via a 22-gauge hypodermic rhythm disorders and apneustic attacks (18). When respiration needle over approximately one minute. For the SHAM group, units are deformed by chemical, pathophysiologic or 0.75 mL of isotonic saline solution was injected instead of mechanical factors, these neural networks initiate the Hering- blood. Six of the ten rabbits subjected to experimental SAH Breuer reflex and affect the pattern of breathing (16,19). So, died within the first week post-surgery and the surviving four ischemic vagal discharges resembling vagal stimulation were followed for 20 days without any medical treatment and may be considered a triggering factor in apneustic attacks then sacrificed. At that point, the lungs and all vagal nerves at the beginning of subarachnoid hemorrhage (SAH). The just over the jugular foramen were removed for histology immunoregulatory role of the vagal nerve on the lungs may examination. Tissues were kept in a 10% formalin solution for be damaged secondary to vagal nerve injury, and respiratory 7 days, following which 1 µm tissue sections were taken and rhythm may be disrupted due to lung inflammation (9). stained with S-100. For the purpose of this study, Schwann cell body necrosis and degenerated axon numbers were the Vagal nerve injury can cause laryngopharyngeal muscle pa- injury criteria of vagal nerves. ralysis, tracheobronchial distortions, reflex vagal bradycardia To estimate the total number of axons of vagal nerves, the and bradypnea (22). In late phase SAH, irreversible axonal fractionation technique was used after the cross-sections injury may mimic a blockade of the vagal nerves. The Hering- of the vagal nerves were obtained according to the basic Breuer reflex may be abolished during acutely developed ce- sampling procedure and stereological principles described rebral ischemia and restored by recovery of ischemic cerebral by Gundersen (10). Axon density of the vagal nerve was processes (1, 20). It is well known that axon density of vagal estimated using an unbiased counting frame of known size. nerves plays an important role in their activities (14). Also, The microscope used had a two attachments; a camera and neuron density of autonomic ganglions strongly affects au- was and a platform with two dial indicators and two arms for tonomic functions (14). So, axon density of vagal nerves may mounting the microscope stage. The two dial indicators (5 µm be an important factor in the regulation of respiration, and resolution) mounted to the microscope measured movement reduced neuron density due to SAH may cause respiration in the x and y planes of the stage. The vagal nerve images disorders and even arrest. In the presented study, it is demon- and measurements obtained were recorded by the camera strated that SAH causes not only cerebral ischemic insult, but and uploaded to a computer and the numbers of living and also brain stem and cranial nerve injuries. We hypothesized degenerated neurons of the vagal nerve of all animals were that ischemic vagal nerve root injury is an important factor in counted. the development of respiratory arrhythmia; a novel concept not previously studied. In order to estimate respiration capacities and depth, respiration-time curves generated by computer were MATERIAL and METHODS overlaid onto minisquare pointed papers in order to facilitate This study was conducted at the Medical Experimental calculations (See Figure 3 for an example). The height of the Research Center, Ataturk University. The Ethical Committee curve from the basal line to the apical points was accepted of Ataturk University approved the study protocol. All as respiration depth and the surface area under the curve procedures were performed in accordance with the National was accepted as respiration capacity per respiration cyclus Institute of Health Principles of Laboratory
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